An Innovative Approach in the Baking of Bread with CO2 Gas Hydrates as Leavening Agents.

Gas (guest) molecules are trapped in hydrogen-bonded water molecules to form gas hydrates (GH), non-stoichiometric solids that resemble ice. High pressure and low temperature are typical conditions for their development, with van der Waals forces joining the host and guest molecules. This article study investigates the application of CO2 gas hydrates (CO2 GH) as a leavening agent in baking, with particular reference to the production of wheat bread. The main intention of this study is to better understand the complex bread dough formed by CO2 GH and its impact on product quality. This may enable the adaptation of CO2 GH in baking applications, such as those that can specifically influence wheat bread properties, and so the final bread quality. The present research further examines the comparative evaluation of yeast bread with the GH bread's impact on bread quality parameters. The amount of GH was varied from 10 to 60%/amount of flour for the GH breads. The GH breads were compared with the standard yeast bread for different quality parameters such as volume, texture, and pore analysis. The results show that the bread with 20% and 40% GH obtained the best results in terms of volume and pore size. Moreover, this article also sheds some light on the future applications of the use of CO2 GH as leavening agents in foods. This knowledge could help to create new procedures and criteria for improved GH selection for applications in bread making and other bakery or food products.

Transgelin is a poor prognostic factor associated with advanced colorectal cancer (CRC) stage promoting tumor growth and migration in a TGFß-dependent manner.

Colorectal cancer (CRC) is the fourth most common cancer type globally. Investigating the signaling pathways that maintain cancer cell phenotype can identify new biomarkers for targeted therapy. Aberrant transforming growth factor-ß (TGFß) signaling has been implicated in CRC progression, however, the exact mechanism by which TGFß exerts its function is still being unraveled. Herein, we investigated TAGLN expression, prognostic value, and its regulation by TGFß in CRC. While TAGLN was generally found to be downregulated in CRC, elevated expression of TAGLN was associated with advanced CRC stage and predicted poor overall survival (hazard ratio (HR) = 1.8, log-rank test P-value = 0.014) and disease-free survival (HR = 1.6, log-rank test P-value = 0.046), hence implicating TAGLN as poor prognostic factor in CRC. Forced expression of TAGLN was associated with enhanced CRC cell proliferation, clonogenic growth, cell migration and in vivo tumor formation in immunocompromised mice, while targeted depletion of TAGLN exhibited opposing biological effects. Global gene expression profiling of TAGLN-overexpressing or TAGLN-deficient CRC cell lines revealed deregulation of multiple cancer-related genes and signaling pathways. Transmission electron microscopy (TEM) revealed ultrastructural changes due to loss of TAGLN, including disruption of actin cytoskeleton organization and aberrant actin filament distribution. Hierarchical clustering, principle component, and ingenuity pathway analyses revealed distinct molecular profile associated with TAGLNhigh CRC patients with remarkable activation of a number of mechanistic networks, including SMARCA4, TGFß1, and P38 MAPK. The P38 MAPK was the top predicted upstream regulator network promoting cell movement through regulation of several intermediate molecules, including TGFß1. Concordantly, functional categories associated with cellular movement and angiogenesis were also enriched in TAGLNhigh CRC, supporting a model for the molecular mechanisms linking TGFß-induced upregulation of TAGLN and CRC tumor progression and suggesting TAGLN as potential prognostic marker associated with advanced CRC pathological stage.

TGFß1-Induced Differentiation of Human Bone Marrow-Derived MSCs Is Mediated by Changes to the Actin Cytoskeleton.

TGFß is a potent regulator of several biological functions in many cell types, but its role in the differentiation of human bone marrow-derived skeletal stem cells (hMSCs) is currently poorly understood. In the present study, we demonstrate that a single dose of TGFß1 prior to induction of osteogenic or adipogenic differentiation results in increased mineralized matrix or increased numbers of lipid-filled mature adipocytes, respectively. To identify the mechanisms underlying this TGFß-mediated enhancement of lineage commitment, we compared the gene expression profiles of TGFß1-treated hMSC cultures using DNA microarrays. In total, 1932 genes were upregulated, and 1298 genes were downregulated. Bioinformatics analysis revealed that TGFßl treatment was associated with an enrichment of genes in the skeletal and extracellular matrix categories and the regulation of the actin cytoskeleton. To investigate further, we examined the actin cytoskeleton following treatment with TGFß1 and/or cytochalasin D. Interestingly, cytochalasin D treatment of hMSCs enhanced adipogenic differentiation but inhibited osteogenic differentiation. Global gene expression profiling revealed a significant enrichment of pathways related to osteogenesis and adipogenesis and of genes regulated by both TGFß1 and cytochalasin D. Our study demonstrates that TGFß1 enhances hMSC commitment to either the osteogenic or adipogenic lineages by reorganizing the actin cytoskeleton.